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. 2022 Mar 4;21:66. doi: 10.1186/s12943-022-01541-9

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© The Author(s) 2022, corrected publication 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — Gilteritinib enhanced the ability of FLT3scFv/NKG2D-CAR T cells in killing AML cells in vitro. A Special cytotoxicity of UTD, FLT3scFv/NKG2D CAR T alone or combined with gilteritinib against AML cells (MOLM-13 and MV4-11) using LDH cytotoxicity assay (4-h co-culture with 10,000 target cells/well). B Annexin V/PI apoptosis assay (48-h co-culture with 2 × 10⁵ target cells/well) showing FLT3scFv/NKG2D-CAR T cells had potent and specific cytotoxicity and apoptotic effects against MOLM-13 and MV4-11 cells. These effects were enhanced by pretreatment with the FLT3 inhibitor gilteritinib. C Flow cytometry analysis showing the percentage of surviving CD33 + AML cells (24-h co-culture of MOLM-13 and MV4-11 with 25,000 cells/well) significantly reduced in the FLT3scFv/NKG2D-CAR T cell group compared with the UTD group in a dose-dependent manner, and the gilteritinib combination treatment group showed a further decrease in the percentage of residual CD33 + AML cells. D ELISA analyses showing IL-2 and IFN-γ secretion by UTD and FLT3scFv/NKG2D-CAR T cells after 24-h incubation with non-treated or pre-treated target cells (MOLM-13 and MV4-11) at an E:T ratio of 5:1 (T cells: 2.5 × 10⁶/well; target cells: 5 × 10⁵/well).The levels of secreted IL-2 and IFN-γ were further increased by gilteritinib pre-treatment for 24 h. E Flow cytometry analysis showed the survival of AML cells from patients with FLT3^mut+ or FLT3^mut− AML (24-h co-culture with 25,000 cells/well) reduced with FLT3scFv/NKG2D-CAR T cell treatment in a dose-dependent manner and further decreased in AML cells pre-treated with gilteritinib. F The diagrams show fewer surviving CD33 + cells in FLT3^mut+ AML cells than in FLT3^mut− cells following FLT3scFv/NKG2D-CAR T cell therapy with or without gilteritinib pre-treatment. G, gilteritinib; LDH, lactate dehydrogenase; UTD: un-transduced CD3 + T cells. * p < 0.05; ** and ## p < 0.01; *** and ### p < 0.001; **** and #### p < 0.0001